Статті в журналах: "Epstein-Barr Virus Burkitt's Lymphoma"

1

Farzanehpour, Mahdieh, Amir M. M. Fard, and Hadi E. G. Ghaleh. "A brief overview of the Epstein Barr virus and its association with Burkitt's lymphoma." Romanian Journal of Military Medicine 125, no. 3 (August 1, 2022): 373–81. http://dx.doi.org/10.55453/rjmm.2022.125.3.4.

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Epstein Barr virus (EBV) is known as an oncovirus and associates with several human malignancies such as Burkitt's lymphoma, other non-Hodgkin lymphomas, nasopharyngeal carcinoma, Hodgkin's disease, gastric adenocarcinoma, etc. in Burkitt's lymphoma, and the key event is the translocation of MYC gene, that increase of cell survival and aberrant expression of MYC gene. The biology of EBV and its function in the development of Burkitt's lymphoma are discussed in this review

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2

Shah, K. M., and L. S. Young. "Epstein–Barr virus and carcinogenesis: beyond Burkitt's lymphoma." Clinical Microbiology and Infection 15, no. 11 (November 2009): 982–88. http://dx.doi.org/10.1111/j.1469-0691.2009.03033.x.

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3

Okano, M., G. M. Thiele, J. R. Davis, H. L. Grierson, and D. T. Purtilo. "Epstein-Barr virus and human diseases: recent advances in diagnosis." Clinical Microbiology Reviews 1, no. 3 (July 1988): 300–312. http://dx.doi.org/10.1128/cmr.1.3.300.

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Since the discovery of Epstein-Barr virus (EBV) from a cultured Burkitt's lymphoma cell line in 1964, the virus has been associated with Burkitt's lymphoma, nasopharyngeal carcinoma, and infectious mononucleosis. During the recent decade, EBV has been etiologically implicated in a broad spectrum of human diseases. The precise role of this virus in these diseases is not well understood, but clearly, defective immunosurveillance against the virus may permit an uncontrolled proliferation of EBV-infected cells. As a result, a growing number of cases of EBV-associated B-cell proliferative diseases or lymphoma have been noted in patients with primary and acquired immunodeficiencies. These lymphoproliferative diseases and others, such as chronic mononucleosis syndrome, are leading to new areas of investigation which are providing information regarding the pathogenetic mechanisms of EBV-induced diseases. The early accurate diagnosis of EBV infection can be achieved by performing EBV-specific serology, detecting for EBV-determined nuclear antigen in tissues, establishing spontaneous lymphoid cell lines, and using molecular hybridization techniques for demonstrating the presence of viral genome in affected lesions.

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4

Tosato, G., C. Sgadari, K. Taga, KD Jones, SE Pike, A. Rosenberg, JM Sechler, IT Magrath, LA Love, and K. Bhatia. "Regression of experimental Burkitt's lymphoma induced by Epstein-Barr virus-immortalized human B cells." Blood 83, no. 3 (February 1, 1994): 776–84. http://dx.doi.org/10.1182/blood.v83.3.776.776.

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Abstract Epstein-Barr virus (EBV)-immortalized human B cells survive only transiently when injected subcutaneously into athymic mice, whereas Burkitt's lymphoma cells give rise to progressively growing subcutaneous tumors. In this study, we tested whether these Burkitt's tumors could be induced to regress via a bystander effect induced by EBV-immortalized B cells. Simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in the same subcutaneous site resulted in tumors that regressed with necrosis and scarring. Similarly, simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in separate subcutaneous sites resulted in regression of a proportion of the Burkitt's tumors. Furthermore, most of the established human Burkitt's tumors regressed with necrosis and scarring after intratumor inoculations with EBV-immortalized B cells. The EBV-immortalized B cells continued to exert this antitumor effect even when killed with irradiation. The experimental approach to Burkitt's lymphoma treatment described here exploits the ability of athymic mice to reject EBV-immortalized B cells to target an effective antitumor response to malignant cells normally incapable of eliciting it.

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5

Tosato, G., C. Sgadari, K. Taga, KD Jones, SE Pike, A. Rosenberg, JM Sechler, IT Magrath, LA Love, and K. Bhatia. "Regression of experimental Burkitt's lymphoma induced by Epstein-Barr virus-immortalized human B cells." Blood 83, no. 3 (February 1, 1994): 776–84. http://dx.doi.org/10.1182/blood.v83.3.776.bloodjournal833776.

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Epstein-Barr virus (EBV)-immortalized human B cells survive only transiently when injected subcutaneously into athymic mice, whereas Burkitt's lymphoma cells give rise to progressively growing subcutaneous tumors. In this study, we tested whether these Burkitt's tumors could be induced to regress via a bystander effect induced by EBV-immortalized B cells. Simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in the same subcutaneous site resulted in tumors that regressed with necrosis and scarring. Similarly, simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in separate subcutaneous sites resulted in regression of a proportion of the Burkitt's tumors. Furthermore, most of the established human Burkitt's tumors regressed with necrosis and scarring after intratumor inoculations with EBV-immortalized B cells. The EBV-immortalized B cells continued to exert this antitumor effect even when killed with irradiation. The experimental approach to Burkitt's lymphoma treatment described here exploits the ability of athymic mice to reject EBV-immortalized B cells to target an effective antitumor response to malignant cells normally incapable of eliciting it.

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6

Stebbing, Justin, and Mark Bower. "Epstein-Barr virus in Burkitt's lymphoma: the missing link." Lancet Oncology 10, no. 4 (April 2009): 430. http://dx.doi.org/10.1016/s1470-2045(09)70045-2.

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7

Kamranvar, S. A., B. Gruhne, A. Szeles, and M. G. Masucci. "Epstein–Barr virus promotes genomic instability in Burkitt's lymphoma." Oncogene 26, no. 35 (February 26, 2007): 5115–23. http://dx.doi.org/10.1038/sj.onc.1210324.

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8

Goldstein, J. A., and R. L. Bernstein. "Burkitt's Lymphoma and the Role of Epstein-Barr Virus." Journal of Tropical Pediatrics 36, no. 3 (June 1, 1990): 114–20. http://dx.doi.org/10.1093/tropej/36.3.114.

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9

Joob, Beuy, and Viroj Wiwanitkit. "Malaria, Epstein-Barr virus, vitamin A and Burkitt's lymphoma." International Journal of Cancer 142, no. 4 (October 31, 2017): 863. http://dx.doi.org/10.1002/ijc.31118.

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10

Sánchez-Giler, Sunny, Alan Herrera-Vásquez, Claudia Castillo-Zambrano, Luis Solórzano-Alava, Dolores Zambrano-Castro, Cristina Kuon-Yeng, Alba Silva-Orellana, Juan Murillo-Zambrano, and Genaro Cucalón-González. "Detección del Virus de Epstein-Barr en linfoma mediante qPCR //Detection of Epstein-Barr Virus (EBV) in lymphoma through qPCR." Ciencia Unemi 11, no. 26 (June 5, 2018): 126. http://dx.doi.org/10.29076/issn.2528-7737vol11iss26.2018pp126-133p.

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Virus Epstein Barr (VEB) ha sido relacionado con una serie de tumores malignos de origen epitelial y linfoide. Existe una clara correlación entre este virus y enfermedades linfoproliferativas como Linfoma de Burkitt (LB), Linfoma Hodgkin (LH), Linfoma no Hodgkin (LNH) y carcinoma gástrico. Se han desarrollado diversas técnicas para la detección de VEB en células tumorales: hibridación in situ (RISH) que detecta RNAs (ácido ribonucleico) pequeños codificados para VEB (EBERs) en las células con infección latente, considerado el estándar de oro para la identificación del virus; la reacción en cadena de la polimerasa (PCR) que permite la detección de la cepa viral y representa un ensayo importarte en el diagnóstico del virus. Se realizó un estudio retrospectivo a partir de muestras de tejidos en parafina de pacientes con linfoma y se buscó al virus mediante PCR y RISH. La prevalencia del virus fue de 58,82%, el género más afectado fue el masculino y el grupo más afectado fue el de 31/40 años. La presencia del virus fue similar en ambos tipos de linfoma: Hodking y No Hodking. La técnica de RISH se mostró más eficiente para detectar la presencia del virus. AbstractEpstein Barr Virus (EBV) is linked to a number of malignant tumors of epithelial and lymphoid origin. There is a strong correlation between this virus and lymphoproliferative diseases such as Burkitt's lymphoma (BL), Hodgkin lymphoma (HL), non-Hodgkin lymphoma (NHL) and gastric carcinoma. There are various techniques developed to detect EBV in tumor cells: in situ hybridization (ISH) detects small coded RNAs (ribonucleic acid) to VEB (EBERs) in latently infected cells. This is considered the gold standard for virus identification. The polymerase chain reaction (PCR) allows the detection of the viral strain and represents an important fact in the virus diagnose. We conducted a retrospective study in paraffin from tissue samples of patients with lymphoma and we sought the virus through PCR and RISH. The virus prevalence was 58.82%, the most affected gender was male and the most affected group was 31/40 years. The virus was similar in both types of lymphoma: Hodgkin and non-Hodgkin. RISH technique seemed to be more efficient to detect the virus.

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11

Shannon-Lowe, Claire, Alan B. Rickinson, and Andrew I. Bell. "Epstein–Barr virus-associated lymphomas." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1732 (September 11, 2017): 20160271. http://dx.doi.org/10.1098/rstb.2016.0271.

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Epstein–Barr virus (EBV), originally discovered through its association with Burkitt lymphoma, is now aetiologically linked to a remarkably wide range of lymphoproliferative lesions and malignant lymphomas of B-, T- and NK-cell origin. Some occur as rare accidents of virus persistence in the B lymphoid system, while others arise as a result of viral entry into unnatural target cells. The early finding that EBV is a potent B-cell growth transforming agent hinted at a simple oncogenic mechanism by which this virus could promote lymphomagenesis. In reality, the pathogenesis of EBV-associated lymphomas involves a complex interplay between different patterns of viral gene expression and cellular genetic changes. Here we review recent developments in our understanding of EBV-associated lymphomagenesis in both the immunocompetent and immunocompromised host. This article is part of the themed issue ‘Human oncogenic viruses’.

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12

Spriggs, D. R. "Cofactors in Disease: Epstein-Barr Virus, Oncogenes, and Burkitt's Lymphoma." Journal of Infectious Diseases 151, no. 5 (May 1, 1985): 977–78. http://dx.doi.org/10.1093/infdis/151.5.977.

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13

Rowe, Martin, Gemma L. Kelly, Andrew I. Bell, and Alan B. Rickinson. "Burkitt's lymphoma: The Rosetta Stone deciphering Epstein-Barr virus biology." Seminars in Cancer Biology 19, no. 6 (December 2009): 377–88. http://dx.doi.org/10.1016/j.semcancer.2009.07.004.

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14

Bell, Andrew, and Alan B. Rickinson. "Epstein–Barr virus, the TCL-1 oncogene and Burkitt's lymphoma." Trends in Microbiology 11, no. 11 (November 2003): 495–97. http://dx.doi.org/10.1016/j.tim.2003.09.009.

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15

Chao, Tsu-Yi, Tow-Yeuan Wang, and Wei-Hua Lee. "Association between Epstein-Barr virus and Burkitt's lymphoma in Taiwan." Cancer 80, no. 1 (July 1, 1997): 121–28. http://dx.doi.org/10.1002/(sici)1097-0142(19970701)80:1<121::aid-cncr16>3.0.co;2-#.

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16

Kuhn-Hallek, I., DR Sage, L. Stein, H. Groelle, and JD Fingeroth. "Expression of recombination activating genes (RAG-1 and RAG-2) in Epstein-Barr virus-bearing B cells [see comments]." Blood 85, no. 5 (March 1, 1995): 1289–99. http://dx.doi.org/10.1182/blood.v85.5.1289.bloodjournal8551289.

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Recombination activating genes 1 and 2 (RAG-1 and RAG-2), are the only lymphoid-specific genes required for the site-directed recombination reaction leading to generation of B-cell receptors and T-cell receptors (TCRs). RAGs are normally expressed during a narrow window of precursor lymphocyte development. RAG expression was examined in Epstein-Barr virus (EBV)-infected B cells. No steady-state RAG RNA was found in EBV immortalized cells, including newly established B lymphoblastoid cell lines derived from precursor lymphocytes that transcribed RAGs at the time of infection. RAG RNAs were detected in some endemic (EBV+) and also in some sporadic (EBV-) Burkitt's lymphoma lines that had been infected with EBV in vitro. The RAG+, EBV+ Burkitt's lines were unusual in that they were SIgM+ (one was SIgG+, SIgM-), CD10+, and lacked terminal deoxynucleotidyl transferase. In EBV+ Burkitt's lymphoma lines, transcription of virus latent membrane protein-1 (LMP-1) was correlated with downregulation of RAG-1 and RAG-2. Conversely, absence of LMP-1 in clones of EBV+ tumor lines was associated with increased RAG transcription. Translocation of c-myc into V(D)J loci has been observed in endemic Burkitt's lymphomas, and heptamer-nonamer recombination signal sequences have been identified at some chromosomal breakpoints. Association of RAG transcription with EBV infection raises the possibility that, under certain conditions, virus might predispose to aberrant V(D)J recombination reactions.

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17

Shirley, Courtney, Nene Kalu, and Richard F. Ambinder. "Nelfinavir Activates Epstein-Barr Virus and Kaposi's Sarcoma Herpesvirus Lytic Cycle by Inducing ER Stress." Blood 118, no. 21 (November 18, 2011): 5011. http://dx.doi.org/10.1182/blood.v118.21.5011.5011.

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Abstract Abstract 5011 Epstein-Barr virus (EBV) and Kaposi's Sarcoma herpesvirus (KSHV) are associated with lymphomas and other malignancies. We previously demonstrated that the proteasome inhibitor, bortezomib, leads to ER stress, induction of the unfolded protein response (UPR), and activation of EBV lytic gene expression.1 Here we investigate nelfinavir, an HIV protease inhibitor that has been reported to induce the UPR.2 Nelfinavir treatment of EBV Burkitt's lymphoma (BL) and KSHV primary effusion lymphoma (PEL) cell lines resulted in changes indicative of ER stress: elevated levels of ATF4, XBP1(s), and CHOP10 (Figure 1), as well as the EBV and KSHV immediate early proteins ZTA and RTA (Figure 2), respectively. The appearance of these UPR markers preceded expression of viral lytic RNAs. Regulated knockdown of Bip, an ER-stress sensor and activator of the UPR, by shRNA inhibited viral lytic RNA induction. These effects were observed using drug levels at or just above the levels achieved with standard clinical dosing of nelfinavir. Gantt et al. have reported that nelfinavir inhibits herpes virion production, including KSHV, in vitro.3 The ability to activate viral gene expression in combination with inhibition of virion production may identify nelfinavir as an especially promising agent for virus-targeted cancer therapies.Figure 1Figure 1. Figure 2Figure 2. Analysis of nelfinavir (NFV) induced ER stress markers by RT-qPCR in Burkitt's lymphoma (Akata) and primary effusion lymphoma (BCBL-1) cells. Analysis of nelfinavir (NFV) induced lytic activation by RT-qPCR in Burkitt's lymphoma (Akata) and primary effusion lymphoma (BCBL-1) cells. Disclosures: No relevant conflicts of interest to declare.

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18

Scarpa, A., L. Borgato, M. Chilosi, P. Capelli, F. Menestrina, F. Bonetti, G. Zamboni, G. Pizzolo, S. Hirohashi, and L. Fiore-Donati. "Evidence of c-myc gene abnormalities in mediastinal large B-cell lymphoma of young adult age [see comments]." Blood 78, no. 3 (August 1, 1991): 780–88. http://dx.doi.org/10.1182/blood.v78.3.780.780.

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Abstract Six cases of mediastinal large B-cell lymphoma (MLCL) with sclerosis were analyzed for the presence and patterns of c-myc and bcl-2 loci rearrangements, and for the presence of Epstein-Barr virus DNA sequences by Southern blot hybridization, c-myc gene alterations were found in three of six cases. Two cases showed the presence of mutations or small rearrangements at the 3′ end of the first exon. The c-myc gene abnormalities found in these two cases are similar to those observed in the translocation 8;14 of the endemic Burkitt's lymphomas or in its variants t(2;8) and t(8;22). A third case showed a major rearrangement of c-myc gene, with truncation within its first intron, similar to those observed in sporadic Burkitt's and in acquired immunodeficiency- associated lymphomas. None of the cases displayed bcl-2 gene rearrangements or contained viral sequences. Our data suggest a possible role for a translocation-mediated c-myc activation in the pathogenesis of MLCL. Conversely, bcl-2 gene and Epstein-Barr virus do not appear to be involved in the pathogenesis of these peculiar lymphomas. The association between c-myc structural modifications and MLCL also seems to be of relevance in light of the peculiar tendency of this tumor to involve unusual extranodal site (eg, kidney), reminiscent of the spreading attitude of Burkitt's limphomas.

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19

Scarpa, A., L. Borgato, M. Chilosi, P. Capelli, F. Menestrina, F. Bonetti, G. Zamboni, G. Pizzolo, S. Hirohashi, and L. Fiore-Donati. "Evidence of c-myc gene abnormalities in mediastinal large B-cell lymphoma of young adult age [see comments]." Blood 78, no. 3 (August 1, 1991): 780–88. http://dx.doi.org/10.1182/blood.v78.3.780.bloodjournal783780.

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Six cases of mediastinal large B-cell lymphoma (MLCL) with sclerosis were analyzed for the presence and patterns of c-myc and bcl-2 loci rearrangements, and for the presence of Epstein-Barr virus DNA sequences by Southern blot hybridization, c-myc gene alterations were found in three of six cases. Two cases showed the presence of mutations or small rearrangements at the 3′ end of the first exon. The c-myc gene abnormalities found in these two cases are similar to those observed in the translocation 8;14 of the endemic Burkitt's lymphomas or in its variants t(2;8) and t(8;22). A third case showed a major rearrangement of c-myc gene, with truncation within its first intron, similar to those observed in sporadic Burkitt's and in acquired immunodeficiency- associated lymphomas. None of the cases displayed bcl-2 gene rearrangements or contained viral sequences. Our data suggest a possible role for a translocation-mediated c-myc activation in the pathogenesis of MLCL. Conversely, bcl-2 gene and Epstein-Barr virus do not appear to be involved in the pathogenesis of these peculiar lymphomas. The association between c-myc structural modifications and MLCL also seems to be of relevance in light of the peculiar tendency of this tumor to involve unusual extranodal site (eg, kidney), reminiscent of the spreading attitude of Burkitt's limphomas.

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20

van den Bosch, Corry. "A Role for RNA Viruses in the Pathogenesis of Burkitt's Lymphoma: The Need for Reappraisal." Advances in Hematology 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/494758.

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Certain infectious agents are associated with lymphomas, but the strength of the association varies geographically, suggesting that local environmental factors make important contributions to lymphomagenesis. Endemic Burkitt’s Lymphoma has well-defined environmental requirements making it particularly suitable for research into local environmental factors. The Epstein-Barr virus and holoendemic Malaria are recognized as important cofactors in endemic Burkitt’s Lymphoma and their contributions are discussed. Additionally, infection with Chikungunya Fever, a potentially oncogenic arbovirus, was associated with the onset of endemic Burkitt’s Lymphoma in one study and also with space-time case clusters of the lymphoma. Chikungunya Virus has several characteristics typical of oncogenic viruses. The Flavivirus, Hepatitis C, a Class 1 Human Carcinogen, closely related to the arboviruses, Yellow Fever, and Dengue, is also more distantly related to Chikungunya Virus. The mechanisms of oncogenesis believed to operate in Hepatitis C lymphomagenesis are discussed, as is their potential applicability to Chikungunya Virus.

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21

Lucchesi, Walter, Gareth Brady, Oliver Dittrich-Breiholz, Michael Kracht, Rainer Russ, and Paul J. Farrell. "Differential Gene Regulation by Epstein-Barr Virus Type 1 and Type 2 EBNA2." Journal of Virology 82, no. 15 (May 14, 2008): 7456–66. http://dx.doi.org/10.1128/jvi.00223-08.

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ABSTRACT A transfection assay with a lymphoblastoid cell line infected with Epstein-Barr virus was used to compare the abilities of type 1 and type 2 EBNA2 to sustain cell proliferation. The reduced proliferation in cells expressing type 2 EBNA2 correlated with loss of expression of some cell genes that are known to be targets of type 1 EBNA2. Microarray analysis of EBNA2 target genes identified a small number of genes that are more strongly induced by type 1 than by type 2 EBNA2, and one of these genes (CXCR7) was shown to be required for proliferation of lymphoblastoid cell lines. The Epstein-Barr virus LMP1 gene was also more strongly induced by type 1 EBNA2 than by type 2, but this effect was transient. Type 1 and type 2 EBNA2 were equally effective at arresting cell proliferation of Burkitt's lymphoma cell lines lacking Epstein-Barr virus and were also shown to cause apoptosis in these cells. The results indicate that differential gene regulation by Epstein-Barr virus type 1 and type 2 EBNA2 may be the basis for the much weaker B-cell transformation activity of type 2 Epstein-Barr virus strains compared to type 1 strains.

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22

Robertson, KD, A. Manns, LJ Swinnen, JC Zong, ML Gulley, and RF Ambinder. "CpG methylation of the major Epstein-Barr virus latency promoter in Burkitt's lymphoma and Hodgkin's disease." Blood 88, no. 8 (October 15, 1996): 3129–36. http://dx.doi.org/10.1182/blood.v88.8.3129.bloodjournal8883129.

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The Epstein-Barr virus (EBV) latency C promoter drives expression of a family of viral proteins commonly targeted by CD8 cytotoxic T cells. These proteins are not generally expressed in African Burkitt's lymphoma and in EBV-associated Hodgkin's disease. The failure to express these proteins is almost certainly an important factor in the evasion of immunosurveillance by EBV-associated tumors. In a previous study, we have shown that transcriptional activation of the C promoter is inhibited by methylation of a particular CpG site upstream of the promoter that prevents binding of a cellular protein (CBF2), and we have shown that this and adjacent CpG sites are methylated in a Burkitt's lymphoma cell line. In the present study, we show that CpG sites in the CBF2 binding region are predominantly methylated in African Burkitt's lymphoma and in EBV-associated Hodgkin's disease. In addition, we present the first direct evidence that the C promoter is transcriptionally silent in Burkitt's lymphoma. In contrast, we show a complete absence of methylation in the CBF2 binding region in a case of reversible EBV-associated B-cell lymphoma arising in an immunocompromised patient whose tumor shows C promoter transcriptional activity. By inhibiting expression of highly antigenic viral proteins, methylation of transcriptional control sequences may veil the presence of virus in tumor tissue from CD8(+) cytotoxic T-cell immune surveillance and thus facilitate viral tumorigenesis.

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23

Brady, G., G. J. MacArthur, and P. J. Farrell. "Epstein-Barr virus and Burkitt lymphoma." Postgraduate Medical Journal 84, no. 993 (July 1, 2008): 372–77. http://dx.doi.org/10.1136/jcp.2007.047977.

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24

Corti, Marcelo, María Florencia Villafañe, Liliana Souto, Ricardo Schtirbu, Marina Narbaitz, and Marcela de Dios Soler. "Burkitt's lymphoma of the duodenum in a patient with AIDS." Revista da Sociedade Brasileira de Medicina Tropical 40, no. 3 (June 2007): 338–40. http://dx.doi.org/10.1590/s0037-86822007000300017.

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Non-Hodgkin's lymphoma of B-cell type is the second most common neoplasm after Kaposi's sarcoma, among patients with human immunodeficiency virus infection. Most non-Hodgkin's lymphoma cases that are associated with acquired immunodeficiency syndrome involve extranodal sites, especially the digestive tract and the central nervous system. We report a case of primary lymphoma of the duodenum in a patient with AIDS. Upper gastrointestinal endoscopy revealed pseudopolypoid masses found in the second portion of the duodenum. A complete diagnostic study including histological, immunohistochemical and virological analyses showed high-grade B-cell Burkitt's lymphoma. The Epstein-Barr virus genome was detected in biopsies by immunohistochemical and in situ hybridization.

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25

Razzouk, B. I., S. Srinivas, C. E. Sample, V. Singh, and J. W. Sixbey. "Epstein-Barr Virus DNA Recombination and Loss in Sporadic Burkitt's Lymphoma." Journal of Infectious Diseases 173, no. 3 (March 1, 1996): 529–35. http://dx.doi.org/10.1093/infdis/173.3.529.

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26

KALIL, J., M. FELLOUS, N. TANIGAKI, F. ROSA, C. PAGNIEZ, C. HERZOG, H. DASTOT, and G. LENOIR. "A new Epstein-Barr virus negative Burkitt's lymphoma derived cell-line." Tissue Antigens 20, no. 1 (December 11, 2008): 47–62. http://dx.doi.org/10.1111/j.1399-0039.1982.tb00328.x.

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27

Gutierrez, M. I., K. Bhatia, and I. Magrath. "Replicative viral DNA in Epstein-Barr virus associated Burkitt's lymphoma biopsies." Leukemia Research 17, no. 3 (March 1993): 285–89. http://dx.doi.org/10.1016/0145-2126(93)90013-b.

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28

Mawson, Anthony R., and Suvankar Majumdar. "Malaria, Epstein-Barr virus infection and the pathogenesis of Burkitt's lymphoma." International Journal of Cancer 141, no. 9 (July 24, 2017): 1849–55. http://dx.doi.org/10.1002/ijc.30885.

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29

Adamson, Amy L. "Epstein-Barr Virus BZLF1 Protein Binds to Mitotic Chromosomes." Journal of Virology 79, no. 12 (June 15, 2005): 7899–904. http://dx.doi.org/10.1128/jvi.79.12.7899-7904.2005.

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ABSTRACT Epstein-Barr virus (EBV) is a human herpesvirus that causes infectious mononucleosis and is associated with several types of cancers, including nasopharyngeal carcinoma and Burkitt's lymphoma. An EBV protein that plays an integral role during lytic replication is the immediate-early protein BZLF1. Our laboratory has found that BZLF1 (Z) localizes to host chromosomes during mitosis. Two Z-interacting proteins are also found localized to mitotic chromosomes in the presence of Z. The association between Z and mitotic chromosomes may lead to the sequestering of Z-interacting proteins within the cell and potentially cause an alteration of chromosome compaction or chromatin structure.

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30

Chatterjee, I., and A. Roy. "Burkitt's Lymphoma in a 5 year old Bengali Girl: A Case Report." Journal of Nepal Paediatric Society 31, no. 1 (January 12, 2011): 61–63. http://dx.doi.org/10.3126/jnps.v31i1.3903.

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Burkitt's lymphoma (BL) is a rare monoclonal proliferation of B-lymphocytes and is classified as a poorly differentiated lymphocytic lymphoma. This tumor was first noted in Africans. The cause of this tumor is debatable, but strong evidence implicates Epstein-Barr virus in its development. This tumor predominantly affects children and is probably the fastest growing tumor in humans, with exuberant proliferation. It is a very rare malignancy accounting for only 0.76% of solid malignant tumors among Indian children. A case of BL of the right hemimandible in a 5-year-old Bengali girl is reported. Key words: Burkitt's lymphoma; Immunohistochemistry; Chemotherapy. DOI: 10.3126/jnps.v31i1.3903J Nep Paedtr Soc 2010;31(1):61-63

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31

Sutkowski, N., T. Palkama, C. Ciurli, R. P. Sekaly, D. A. Thorley-Lawson, and B. T. Huber. "An Epstein-Barr virus-associated superantigen." Journal of Experimental Medicine 184, no. 3 (September 1, 1996): 971–80. http://dx.doi.org/10.1084/jem.184.3.971.

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More than 90% of adults are latently infected with Epstein-Barr virus (EBV), the causative agent of infectious mononucleosis, a self-limiting lymphoproliferative disease characterized by extensive T cell activation. Reactivation of this herpesvirus during immunosuppression is often associated with oncogenesis. These considerations led us to analyze the early events that occur after exposure of the immune system to EBV. Strong major histocompatibility complex (MHC) class II-dependent but not MHC-restricted, T cell proliferation was observed in vitro in response to autologous, lytically infected EBV-transformed B cells. By measuring the appearance of the early activation marker CD69 on individual T cell V beta subsets, we could demonstrate selective activation of human V beta 13- T cells. This was confirmed with murine T cell hybridomas expressing various human BV genes. While EBV- Burkitt's lymphoma cells were nonstimulatory, they induced V beta-restricted T cell activation after EBV infection. EBV specific activation was also demonstrated in cord blood cells, excluding a recall-antigen response. Thus, all of the characteristics of a superantigen-stimulated response are seen, indicating that induction of the EBV lytic cycle is associated with the expression of a superantigen in B cells. A model is presented proposing a role for the superantigen in infection, latency, and oncogenesis.

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32

Maruo, Seiji, Asuka Nanbo, and Kenzo Takada. "Replacement of the Epstein-Barr Virus Plasmid with the EBER Plasmid in Burkitt's Lymphoma Cells." Journal of Virology 75, no. 20 (October 15, 2001): 9977–82. http://dx.doi.org/10.1128/jvi.75.20.9977-9982.2001.

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ABSTRACT Transfection of an Epstein-Barr virus (EBV)-encoded plasmid containing EBER caused a substantial decrease in the level of plasmid containing EBV in Akata and Mutu Burkitt's lymphoma (BL) lines, but failed to do so in other BL lines. The results suggest that EBER could replace the role of EBV, but other EBV products also play a role in the growth of BL.

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33

Grasser, FA, PG Murray, E. Kremmer, K. Klein, K. Remberger, W. Feiden, G. Reynolds, G. Niedobitek, LS Young, and N. Mueller-Lantzsch. "Monoclonal antibodies directed against the Epstein-Barr virus-encoded nuclear antigen 1 (EBNA1): immunohistologic detection of EBNA1 in the malignant cells of Hodgkin's disease." Blood 84, no. 11 (December 1, 1994): 3792–98. http://dx.doi.org/10.1182/blood.v84.11.3792.bloodjournal84113792.

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Monoclonal antibodies directed against the Epstein-Barr virus nuclear protein 1 (EBNA1) were used to examine conventional paraffin sections from a series of EBV-associated lymphoproliferative disorders by immunohistochemistry. The presence of latent EBV infection in tumor cells was determined by in situ hybridization for the Epstein-Barr virus early RNAs (EBERs). Of those EBER-positive cases a total of 28 of 40 cases of Hodgkin's disease, 3 of 3 cases of Burkitt's lymphoma, and 8 of 8 cases of human immunodeficiency virus-associated cerebral B-cell lymphoma expressed detectable amounts of EBNA1. In the positive cases, expression was confined to the tumor cells. No reactivity was detected in EBV-negative cases of the above tumors or in 8 cases of EBV-negative cases of large cell anaplastic non-Hodgkin lymphoma. This report provides the first unequivocal evidence for the expression of the EBNA1 protein in the tumor cells of Hodgkin's disease and validates an important reagent with which to analyze the role of EBV in various virus-associated malignancies.

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34

Delecluse, HJ, M. Raphael, JP Magaud, P. Felman, IA Alsamad, GW Bornkamm, and GM Lenoir. "Variable morphology of human immunodeficiency virus-associated lymphomas with c-myc rearrangements. The French Study Group of Pathology for Human Immunodeficiency Virus-Associated Tumors, I." Blood 82, no. 2 (July 15, 1993): 552–63. http://dx.doi.org/10.1182/blood.v82.2.552.552.

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Abstract Burkitt lymphoma (BL) and immunoblastic lymphoma (IL) are the most frequent lymphoid tumors encountered in human immunodeficiency virus (HIV)-infected patients. Tumors with a morphology intermediate between BL and IL, and the existence of Burkitt's type translocations in some IL cases makes the classification of these tumors sometimes unclear. We have studied 14 cases of BL and IL in HIV-seropositive individuals with regard to clonality, Epstein-Barr virus (EBV) association, and the presence of c-myc rearrangement. Of seven tumors with morphology of BL, all were monoclonal, six showed a c-myc rearrangement and four were associated with EBV. Five tumors with morphology of IL were associated with EBV and devoid of c-myc rearrangement. Three were polyclonal representing EBV-driven lymphoproliferations similar to those observed in transplant recipients. Two tumors, one with a morphology of IL and the other intermediate between IL and BL were monoclonal, associated with EBV, and harbored a c-myc rearrangement. We propose that these last two tumors represent cases of BL that have adopted an immunoblastic morphotype in the context of acquired immunodeficiency syndrome (AIDS), reflecting the morphologic evolution of Burkitt lymphoma cells observed in culture.

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35

Delecluse, HJ, M. Raphael, JP Magaud, P. Felman, IA Alsamad, GW Bornkamm, and GM Lenoir. "Variable morphology of human immunodeficiency virus-associated lymphomas with c-myc rearrangements. The French Study Group of Pathology for Human Immunodeficiency Virus-Associated Tumors, I." Blood 82, no. 2 (July 15, 1993): 552–63. http://dx.doi.org/10.1182/blood.v82.2.552.bloodjournal822552.

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Анотація:

Burkitt lymphoma (BL) and immunoblastic lymphoma (IL) are the most frequent lymphoid tumors encountered in human immunodeficiency virus (HIV)-infected patients. Tumors with a morphology intermediate between BL and IL, and the existence of Burkitt's type translocations in some IL cases makes the classification of these tumors sometimes unclear. We have studied 14 cases of BL and IL in HIV-seropositive individuals with regard to clonality, Epstein-Barr virus (EBV) association, and the presence of c-myc rearrangement. Of seven tumors with morphology of BL, all were monoclonal, six showed a c-myc rearrangement and four were associated with EBV. Five tumors with morphology of IL were associated with EBV and devoid of c-myc rearrangement. Three were polyclonal representing EBV-driven lymphoproliferations similar to those observed in transplant recipients. Two tumors, one with a morphology of IL and the other intermediate between IL and BL were monoclonal, associated with EBV, and harbored a c-myc rearrangement. We propose that these last two tumors represent cases of BL that have adopted an immunoblastic morphotype in the context of acquired immunodeficiency syndrome (AIDS), reflecting the morphologic evolution of Burkitt lymphoma cells observed in culture.

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36

Hammerschmidt, Wolfgang, and Bill Sugden. "Epstein–Barr virus sustains Burkitt's lymphomas and Hodgkin's disease." Trends in Molecular Medicine 10, no. 7 (July 2004): 331–36. http://dx.doi.org/10.1016/j.molmed.2004.05.006.

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37

V, Gurtsevitch. "Epstein-Barr Virus (EBV) Genome Sequence Variations, Virus Strain Classifications and EBV-Associated Tumors." Virology & Immunology Journal 5, no. 1 (January 12, 2021): 1–3. http://dx.doi.org/10.23880/vij-16000269.

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The Epstein-Barr virus (EBV), a member of the Herpesviridae family, belonging to the Gammaherpesvirinae subfamily, has been associated with several nonmalignant and malignant diseases, including Burkitt’s lymphoma, gastric cancer, Hodgkin’s lymphoma, and nasopharyngeal carcinoma. In recent years numerous EBV genome sequences have been analyzed to answer the question of whether EBV genome variations are tumor-specific, ethnically or geographically determined. A clear answer regarding the "specialization" of EBV strains has not yet been received; however, attempts are being made to identify high-risk EBV strains. This mini-review analyzes the most well-known EBV classifications, EBV sequence variations and their association with EBV-associated human pathologies.

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38

Hecht, Jonathan L., and Jon C. Aster. "Molecular Biology of Burkitt’s Lymphoma." Journal of Clinical Oncology 18, no. 21 (November 1, 2000): 3707–21. http://dx.doi.org/10.1200/jco.2000.18.21.3707.

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The diagnostic category of Burkitt’s lymphoma encompasses a closely related group of aggressive B-cell tumors that includes sporadic, endemic, and human immunodeficiency virus–associated subtypes. All subtypes are characterized by chromosomal rearrangements involving the c-myc proto-oncogene that lead to its inappropriate expression. This review focuses on the roles of c-myc dysregulation and Epstein-Barr virus infection in Burkitt’s lymphoma. Although the normal function of c-Myc remains enigmatic, recent data indicate that it has a central role in several fundamental aspects of cellular biology, including proliferation, differentiation, metabolism, apoptosis, and telomere maintenance. We discuss new insights into the molecular mechanisms of these c-Myc activities and their potential relevance to the pathogenesis of Burkitt’s lymphoma and speculate on the role of Epstein-Barr virus.

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39

Aman, P., J. Gordon, N. Lewin, M. Nordström, B. Ehlin-Henriksson, G. Klein, and A. Carstensson. "Surface marker characterization of EBV target cells in normal blood and tonsil B lymphocyte populations." Journal of Immunology 135, no. 4 (October 1, 1985): 2362–67. http://dx.doi.org/10.4049/jimmunol.135.4.2362.

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Abstract Human FACS-sorted B lymphocyte subpopulations were investigated for their susceptibility to immortalization by Epstein Barr virus (EBV). Only B cells reacting with the monoclonal antibody B2 were immortalized, whereas cells reacting with anti-human IgG or the monoclonal antibody BB2 were not responding. Cells positive or negative for IgM, IgD, Burkitt's lymphoma antigen (BLA), BB1, and HB2 were all transformed by EBV.

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40

Niedobitek, G., A. Agathanggelou, M. Rowe, EL Jones, DB Jones, P. Turyaguma, J. Oryema, DH Wright, and LS Young. "Heterogeneous expression of Epstein-Barr virus latent proteins in endemic Burkitt's lymphoma." Blood 86, no. 2 (July 15, 1995): 659–65. http://dx.doi.org/10.1182/blood.v86.2.659.bloodjournal862659.

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Epstein-Barr virus (EBV)-infected cells may sustain three distinct forms of virus latency. In lymphoblastoid cell lines, six EBV-encoded nuclear antigens (EBNA1, 2, 3A, 3B, 3C, -LP), three latent membrane proteins (LMP1, 2A, 2B), and two nuclear RNAs (EBERs) are expressed. This form of latency, termed latency III, is also encountered in some posttransplant lymphoproliferative disorders. In EBV-positive cases of Hodgkin's disease, the EBERs, EBNA1, and the LMPs are expressed (latency II), whereas in Burkitt's lymphoma (BL) only the EBERs and EBNA1 have been detected (latency I). We have studied the expression of EBV proteins in 17 cases of EBV-positive endemic BL by immunohistology. Expression of LMP1 was seen in variable proportions of tumor cells in two cases and EBNA2 was detected in some tumor cells in three other cases. Also, the BZLF1 trans-activator protein was expressed in a few tumor cells in 6 cases, indicating entry into the lytic cycle. A phenotypic drift from latency I to latency III has been observed previously in some BL cell lines. Our results suggest that a similar phenomenon may occur in BL in vivo and indicate that the operational definition of EBV latencies is not easily applied to human tumors.

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41

Osato, T., S. Imai, S. Koizumi, F. Mizuno, T. Aya, T. Kinoshita, H. Tokuda, et al. "AFRICAN BURKITT'S LYMPHOMA AND AN EPSTEIN-BARR VIRUS-ENHANCING PLANT EUPHORBIA TRIUCALLI." Lancet 329, no. 8544 (May 1987): 1257–58. http://dx.doi.org/10.1016/s0140-6736(87)92700-0.

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42

Katzman, Rebecca B., and Richard Longnecker. "Cholesterol-dependent infection of Burkitt's lymphoma cell lines by Epstein–Barr virus." Journal of General Virology 84, no. 11 (November 1, 2003): 2987–92. http://dx.doi.org/10.1099/vir.0.19252-0.

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43

Rowe, M., C. M. Rooney, C. F. Edwards, G. M. Lenoir, and A. B. Rickinson. "Epstein-Barr virus status and tumour cell phenotype in sporadic Burkitt's lymphoma." International Journal of Cancer 37, no. 3 (March 15, 1986): 367–73. http://dx.doi.org/10.1002/ijc.2910370307.

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44

Boyle, MJ, WA Sewell, TB Sculley, A. Apolloni, JJ Turner, CE Swanson, R. Penny, and DA Cooper. "Subtypes of Epstein-Barr virus in human immunodeficiency virus- associated non-Hodgkin lymphoma." Blood 78, no. 11 (December 1, 1991): 3004–11. http://dx.doi.org/10.1182/blood.v78.11.3004.3004.

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Abstract Biopsy samples obtained from 20 patients with human immunodeficiency virus (HIV)-associated non-Hodgkin lymphoma (NHL) were assessed for evidence of Epstein-Barr virus (EBV) and HIV sequences. DNA was extracted from formalin-fixed, paraffin-embedded NHL tissue and specific viral gene sequences were sought using the polymerase chain reaction (PCR). EBV sequences were found in 10 NHL samples (50%), with five tumors showing A-type and five B-type sequences. By serologic testing, 18 of 19 patients had antibodies to EBV, with 14 patients having antibodies to A-type EBV and 11 to B-type EBV. Serology confirmed the high prevalence of type B EBV in HIV-infected patients, but was not a reliable indicator of the EBV subtype present in the lymphomas. HIV sequences were present in biopsy tissue but at a level consistent with an origin from bystander HIV-infected cells. All 20 patients were negative by enzyme-linked immunosorbent assay for antibodies to human T-cell leukemia virus-type I. The high prevalence of type B EBV in these tumors is similar to the findings in endemic Burkitt's lymphoma, where 40% of the tumors have type B viral sequences. In normal populations, type B EBV is rarely found outside the nasopharynx. These studies support the hypothesis that EBV is an important cofactor in NHL in HIV-infected persons. The finding that B- type EBV is present in 25% of HIV-associated NHL suggests that this EBV subtype may be an important human pathogen with a wider geographic distribution than originally thought.

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45

Boyle, MJ, WA Sewell, TB Sculley, A. Apolloni, JJ Turner, CE Swanson, R. Penny, and DA Cooper. "Subtypes of Epstein-Barr virus in human immunodeficiency virus- associated non-Hodgkin lymphoma." Blood 78, no. 11 (December 1, 1991): 3004–11. http://dx.doi.org/10.1182/blood.v78.11.3004.bloodjournal78113004.

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Анотація:

Biopsy samples obtained from 20 patients with human immunodeficiency virus (HIV)-associated non-Hodgkin lymphoma (NHL) were assessed for evidence of Epstein-Barr virus (EBV) and HIV sequences. DNA was extracted from formalin-fixed, paraffin-embedded NHL tissue and specific viral gene sequences were sought using the polymerase chain reaction (PCR). EBV sequences were found in 10 NHL samples (50%), with five tumors showing A-type and five B-type sequences. By serologic testing, 18 of 19 patients had antibodies to EBV, with 14 patients having antibodies to A-type EBV and 11 to B-type EBV. Serology confirmed the high prevalence of type B EBV in HIV-infected patients, but was not a reliable indicator of the EBV subtype present in the lymphomas. HIV sequences were present in biopsy tissue but at a level consistent with an origin from bystander HIV-infected cells. All 20 patients were negative by enzyme-linked immunosorbent assay for antibodies to human T-cell leukemia virus-type I. The high prevalence of type B EBV in these tumors is similar to the findings in endemic Burkitt's lymphoma, where 40% of the tumors have type B viral sequences. In normal populations, type B EBV is rarely found outside the nasopharynx. These studies support the hypothesis that EBV is an important cofactor in NHL in HIV-infected persons. The finding that B- type EBV is present in 25% of HIV-associated NHL suggests that this EBV subtype may be an important human pathogen with a wider geographic distribution than originally thought.

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46

Ali, Abdelwahid Saeed, Mubarak Al-Shraim, Ahmed Musa Al-Hakami, and Ian M. Jones. "Epstein- Barr Virus: Clinical and Epidemiological Revisits and Genetic Basis of Oncogenesis." Open Virology Journal 9, no. 1 (November 3, 2015): 7–28. http://dx.doi.org/10.2174/1874357901509010007.

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Epstein-Barr virus (EBV) is classified as a member in the orderherpesvirales, familyherpesviridae, subfamilygammaherpesvirinaeand the genuslymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL).In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancies

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47

Crawford, Dorothy H. "Biology and disease associations of Epstein–Barr virus." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1408 (April 29, 2001): 461–73. http://dx.doi.org/10.1098/rstb.2000.0783.

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Epstein–Barr virus (EBV) is a human herpesvirus which infects almost all of the world's population subclinically during childhood and thereafter remains in the body for life. The virus colonizes antibody–producing (B) cells, which, as relatively long–lived resting cells, are an ideal site for long–term residence. Here EBV evades recognition and destruction by cytotoxic T cells. EBV is passed to naive hosts in saliva, but how the virus gains access to this route of transmission is not entirely clear. EBV carries a set of latent genes that, when expressed in resting B cells, induce cell proliferation and thereby increase the chances of successful virus colonization of the B–cell system during primary infection and the establishment of persistence. However, if this cell proliferation is not controlled, or if it is accompanied by additional genetic events within the infected cell, it can lead to malignancy. Thus EBV acts as a step in the evolution of an ever–increasing list of malignancies which are broadly of lymphoid or epithelial cell origin. In some of these, such as B–lymphoproliferative disease in the immunocompromised host, the role of the virus is central and well defined; in others, such as Burkitt's lymphoma, essential cofactors have been identified which act in concert with EBV in the evolution of the malignant clone. However, in several diseases in which the presence of EBV has more recently been discovered, the role of the virus is unclear. This review describes recent views on the EBV life cycle and its interlinks with normal B–cell biology, and discusses how this interrelationship may be upset and result in EBV–associated disease.

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48

Murray, Paul G., and Lawrence S. Young. "Epstein–Barr virus infection: basis of malignancy and potential for therapy." Expert Reviews in Molecular Medicine 3, no. 28 (November 15, 2001): 1–20. http://dx.doi.org/10.1017/s1462399401003842.

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The Epstein–Barr virus (EBV) is a human herpesvirus that is usually carried lifelong as an asymptomatic infection. EBV is the causative agent of infectious mononucleosis and has been linked to the development of several malignant tumours, including B-cell neoplasms such as Burkitt's lymphoma and Hodgkin's disease, certain forms of T-cell lymphoma, and some epithelial tumours, such as undifferentiated nasopharyngeal carcinoma and a proportion of gastric cancers. All these tumours are characterised by the presence of multiple extrachromosomal copies of the circular viral genome in the tumour cells and the expression of EBV-encoded latent genes, which appear to contribute to the malignant phenotype. An increasing understanding of the function of EBV latent genes and of the nature of the immune response to the virus is providing exciting new possibilities for the treatment of EBV-associated malignancies. For example, adoptive transfer of virus-specific cytotoxic T lymphocytes has already been of value in the treatment of EBV-positive B-cell lymphomas arising in post-transplant patients, and this approach is currently being investigated in other EBV-associated tumours. In addition, gene therapy offers the opportunity to deliver agents that might directly interfere with the function of specific EBV genes. This review summarises the role of EBV in malignancy. In particular, it focuses on the latent proteins as a basis for understanding how EBV might contribute to the process of transformation. Strategies to target EBV in tumours, potentially providing alternative therapeutic approaches, are also discussed.

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49

Su, IJ, HC Hsieh, KH Lin, WC Uen, CL Kao, CJ Chen, AL Cheng, ME Kadin, and JY Chen. "Aggressive peripheral T-cell lymphomas containing Epstein-Barr viral DNA: a clinicopathologic and molecular analysis." Blood 77, no. 4 (February 15, 1991): 799–808. http://dx.doi.org/10.1182/blood.v77.4.799.799.

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Abstract The Epstein-Barr virus (EBV) has been shown to be associated with posttransplant lymphoma, Hodgkin's disease, and T-cell lymphoma, in addition to African Burkitt's lymphoma. In a retrospective study of 56 consecutive cases of T-cell lymphoma, EBV DNA was found by Southern blot and in situ DNA hybridization in 10 (20%) of 50 peripheral T-cell lymphomas, but in none of six cases of T-lymphoblastic lymphoma. Peripheral T-cell lymphomas containing EBV DNA could be subclassified into three categories according to histology and immunophenotypic studies: (1) T-cell lymphoma of the helper phenotype, five cases. Two cases had histologic features resembling angioimmunoblastic lymphadenopathy (AILD). (2) T-cell lymphoma of the cytotoxic/suppressor phenotype, four cases. AILD-like features could also be recognized in two cases. Reed-Sternberg-like giant cells were identified in three cases designated Hodgkin-like T-cell lymphoma. (3) Angiocentric T-cell lymphoma or lymphomatoid granulomatosis in one case, initially affecting the skin and nose; no T-cell subset could be defined. Six of the eight EBV DNA-positive patients tested for serum EBV antibodies had elevated titers of IgG antiviral capsid antigen (greater than 640) and/or early antigen (greater than 10). From combined studies of Southern blot hybridization by using EBV termini fragment probe and in situ DNA hybridization, the EBV genomes appeared to be clonotypically proliferated in the neoplastic T cells. The patients in all three groups usually had prolonged fever preceding the diagnosis, hepatosplenomegaly, an aggressive clinical course, and poor response to chemotherapy; nine died with a median survival of only 8 months. We propose that these EBV-associated aggressive T-cell lymphomas, like human T-cell leukemia/lymphoma virus-positive T-cell lymphoma, have characteristic clinicopathologic features and should be treated as a separate disease entity.

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50

Su, IJ, HC Hsieh, KH Lin, WC Uen, CL Kao, CJ Chen, AL Cheng, ME Kadin, and JY Chen. "Aggressive peripheral T-cell lymphomas containing Epstein-Barr viral DNA: a clinicopathologic and molecular analysis." Blood 77, no. 4 (February 15, 1991): 799–808. http://dx.doi.org/10.1182/blood.v77.4.799.bloodjournal774799.

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Анотація:

The Epstein-Barr virus (EBV) has been shown to be associated with posttransplant lymphoma, Hodgkin's disease, and T-cell lymphoma, in addition to African Burkitt's lymphoma. In a retrospective study of 56 consecutive cases of T-cell lymphoma, EBV DNA was found by Southern blot and in situ DNA hybridization in 10 (20%) of 50 peripheral T-cell lymphomas, but in none of six cases of T-lymphoblastic lymphoma. Peripheral T-cell lymphomas containing EBV DNA could be subclassified into three categories according to histology and immunophenotypic studies: (1) T-cell lymphoma of the helper phenotype, five cases. Two cases had histologic features resembling angioimmunoblastic lymphadenopathy (AILD). (2) T-cell lymphoma of the cytotoxic/suppressor phenotype, four cases. AILD-like features could also be recognized in two cases. Reed-Sternberg-like giant cells were identified in three cases designated Hodgkin-like T-cell lymphoma. (3) Angiocentric T-cell lymphoma or lymphomatoid granulomatosis in one case, initially affecting the skin and nose; no T-cell subset could be defined. Six of the eight EBV DNA-positive patients tested for serum EBV antibodies had elevated titers of IgG antiviral capsid antigen (greater than 640) and/or early antigen (greater than 10). From combined studies of Southern blot hybridization by using EBV termini fragment probe and in situ DNA hybridization, the EBV genomes appeared to be clonotypically proliferated in the neoplastic T cells. The patients in all three groups usually had prolonged fever preceding the diagnosis, hepatosplenomegaly, an aggressive clinical course, and poor response to chemotherapy; nine died with a median survival of only 8 months. We propose that these EBV-associated aggressive T-cell lymphomas, like human T-cell leukemia/lymphoma virus-positive T-cell lymphoma, have characteristic clinicopathologic features and should be treated as a separate disease entity.

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